The management of cardiovascular stability in shock patients is of paramount importance in critical care. New, cutting edge knowledge is necessary to overcome the shortcomings of available therapies, in order to cope with the challenges that anesthesiologists, intensive care specialists and emergency physicians face when dealing with shock patients.
Current therapies are targeted to reduce symptoms of shock and multiple organ failure, but they are unable to target the root cause or to act at the “beginning of the cascade”, because of the lack of a model explaining the molecular basis of shock induced tissue injury and ensuing multiple organ failure. Hence, the effectiveness of anti-hypotensive interventions such as fluid resuscitation is limited. Fluid may restore blood pressure within minutes, but complications such as pulmonary edema may arise on a longer time scale in patients who are unresponsive to fluid infusion, and cause more severe stress to the patient’s hemodynamic stability, respiratory efficiency, and immune system.
This proposal seeks to shed light on the molecular trigger of acute heart failure in association to shock, in the presence of uncontrolled proteolytic activity, in order to identify inflammatory mediators and markers which are activated in shock, through a systematic analysis of expression levels of genes and their protein products, and novel targets for the delivery of new therapies, necessary to overcome the limitations of current ones.
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